Tendon injuries constitute an increasing proportion of trauma cases reported at our hospital, yet research in the molecular biology of tendon healing has been neglected. The major response of cells in an injured tendon is to produce new collagen and noncollagen proteins. Collagen is the key structural protein that persists, giving tendon its ability to resist tensile forces. The collagen crosslink content and location largely determine themagnitude of the resistance to tensile force. It is known that immobilization of an injured limb leads to joint stiffness and intractable adhesions in ligaments and tendons that impair mobility. An increase in metastable, reducible collagen crosslinks accompanies loss of mobility. Middle exercise of an injured tendon as early as possible after surgical repair is favorable to healing because certain metastable, reducible, and stable pyridinoline crosslinks may not form to limit motion. How do tendon cells react to and regulate their collagen and noncollagen protein responses to wounding, and how does immobiliztion or motion alter these responses? How do sheath, synovial cells, and inner tendon fibroblasts interact with each other to produce sufficient quantities of the appropriate collagen that has the right qualities? Are certain combinations of these cells involved in matrix reorganiztion during healing and which of these cells has the greatest role? During the course of this research, we have found tht fibronectin production and secretion is increased in synovial cells compared to internal fibroblasts both in vivo and in vitro? Is fibronectin used as a cell attachment molecule alone by these cells and could abnormal secretion promote adhesion formation? Is firbonectin found in conjunction with some other molecule such as hyaluronic acid on the tendon surface to act as a lubricant? Will immobilization and motion alter fibronectin synthesis and secretion by tendon cell populations? The overall objectives of this study are to identify changes in the structure of collagen in tendons that are healing and have been subjected to immobilization or motion and to investigate the biochemical responses of tendon cells in vivo and in vitro to applied forces. Based on results of animal experimentation, we hope to apply a strategy to human medicine involving physical and chemical intervention to improve tendon healing.